Skeletal trauma and other serious illnesses result in excessive loss of skeletal muscle protein as well as a myriad of metabolic alterations. In this study, the oxidation of the branched-chain amino acid leucine by the traumatized, oral fed rat was investigated. Bilateral femoral fracture did not change the oxidational rate at 24 hrs but increased it 100% above control on day 2. The rate gradually fell being 56% and 17% increased on days 3 and 4, respectively. The traumatized rats have less nitrogen retention on all seven days of the study. In an associated study, total parenteral feeding was found to elevate the oxidation of leucine by 80-85% when compared to oral fed rats. This increase in leucine oxidation was comparable to that observed for traumatized rats except that oxidation of leucine by health TPN fed rats remained elevated for 7 days. Comparative data on leucine oxidation during skeletal fractures in humans have shown that men increase leucine oxidation by 300% after injury and that women increase leucine oxidation by 100% post trauma. This sex difference in the metabolic response to injury is also observed for urinary nitrogen excretion, whole body protein kinetics and urea metabolism. The mechanism behind this difference is unknown. The data obtained from leucine oxidation by humans and rats suggests that the rat model of trauma is adequate for investigating changes in amino acid metabolism after injury.